An experimental sub-human primate model of central pain has been discovered. Macaques have been observed to predictably mutilate their hinklimb after undergoing a contralateral midthoracic anterolateral cordotomy or hemisection. This remarkable phenomenon is reminiscent of the disturbing paresthesias which have been described in man after similar spinal surgery, and also after mesencephalic tractotomy, or in cases of a certain thalamic lesion. The macaques exhibit no motor loss, and only a moderate hypalgesia is evident. The sensory disturbance is objectified by self-mutilation. The objective is to analyze the morpho-physiology of this phenomena by: 1) varying the level of the lesion (spinal cord, mesencephalon, and diencephalon); 2) interupting other neural structures (spinal cord or sympathetic trunk), in combination with the inciting lesion; and 3) analyzing the microphysiology of the neural activity in the sensory cortex when there exists an inciteful lesion. Results will be conceptualized in terms of: 1) the pathway, which when destroyed, produces this phenomenon; 2) the mechanisms which sustain normal and abnormal pain; and 3) the influence of these upon cortical function.